Strep throat causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S [2]

Overview

Strep throat is caused by B hemolytic Group A streptococcal infection. More than 80 serotypes are identified based on M protien. GAS strep throat may be associated with serotypes such as M types 1, 3, 5, 6, 14, 18, 19, and 24.^[1]

Causes

Strep throat is caused by B hemolytic Group A streptococcal infection.

Reservoir

Members of the normal flora
Human skin and mucous membrane are the only known reservoirs

Serovars

More than 80 serotypes identified based on M protien
GAS strep throat may be associated with serotypes such as M types 1, 3, 5, 6, 14, 18, 19, and 24.^[1]^[2]^[3]

Features of group A streptococcal infection

Gram-positive coccus (grows in chains)
Non-motile
Non-spore forming
0.5-1.2µm in size
Catalase-negative
Facultative anaerobes or obligate (strict) anaerobes
Requires enriched media (blood agar) to grow
Capsulated (hyaluronic acid capsule)

Classification of GAS

According to the Lancefield classification, based on the group A antigen in the cell wall, it is named group A streptococcus
Based on the hemolysis on blood agar, the GAS is β-hemolytic (clear, complete lysis of red cells)

Virulence factors

Virulence factors of group A streptococci include:^[4]^[5]

A hyaluronic acid capsule (outermost covering inhibits phagocytosis)
Peptidoglycan cell wall
Cell membrane
Adhesion molecules

M protein PMC358122
Lipoteichoic acid (located in cell membrane)

Toxins

Pyrogenic (erythrogenic) toxin (rash of scarlet fever)

Cytolysins

Streptokinase
Streptodornase (DNase B)
Streptolysins
Hyaluronidase

References

↑ ^1.0 ^1.1 Fischetti VA (1989). “Streptococcal M protein: molecular design and biological behavior”. Clin Microbiol Rev. 2 (3): 285–314. PMC 358122. PMID 2670192.
↑ Cunningham MW (2000). “Pathogenesis of group A streptococcal infections”. Clin Microbiol Rev. 13 (3): 470–511. PMC 88944. PMID 10885988.
↑ Stanley J, Desai M, Xerry J, Tanna A, Efstratiou A, George R (1996). “High-resolution genotyping elucidates the epidemiology of group A streptococcus outbreaks”. J Infect Dis. 174 (3): 500–6. PMID 8769606.
↑ Smeesters PR, McMillan DJ, Sriprakash KS (2010). “The streptococcal M protein: a highly versatile molecule”. Trends Microbiol. 18 (6): 275–82. doi:10.1016/j.tim.2010.02.007. PMID 20347595.
↑ Mora M, Bensi G, Capo S, Falugi F, Zingaretti C, Manetti AG; et al. (2005). “Group A Streptococcus produce pilus-like structures containing protective antigens and Lancefield T antigens”. Proc Natl Acad Sci U S A. 102 (43): 15641–6. doi:10.1073/pnas.0507808102. PMC 1253647. PMID 16223875.

Template:WH Template:WS

[pmid2670192-1] 1.0 ^1.1 Fischetti VA (1989). “Streptococcal M protein: molecular design and biological behavior”. Clin Microbiol Rev. 2 (3): 285–314. PMC 358122. PMID 2670192.

[pmid10885988-2] Cunningham MW (2000). “Pathogenesis of group A streptococcal infections”. Clin Microbiol Rev. 13 (3): 470–511. PMC 88944. PMID 10885988.

[pmid8769606-3] Stanley J, Desai M, Xerry J, Tanna A, Efstratiou A, George R (1996). “High-resolution genotyping elucidates the epidemiology of group A streptococcus outbreaks”. J Infect Dis. 174 (3): 500–6. PMID 8769606.

[pmid20347595-4] Smeesters PR, McMillan DJ, Sriprakash KS (2010). “The streptococcal M protein: a highly versatile molecule”. Trends Microbiol. 18 (6): 275–82. doi:10.1016/j.tim.2010.02.007. PMID 20347595.

[pmid16223875-5] Mora M, Bensi G, Capo S, Falugi F, Zingaretti C, Manetti AG; et al. (2005). “Group A Streptococcus produce pilus-like structures containing protective antigens and Lancefield T antigens”. Proc Natl Acad Sci U S A. 102 (43): 15641–6. doi:10.1073/pnas.0507808102. PMC 1253647. PMID 16223875.

[1]

[2]

[3]

[4]

[5]